[Accidental hypothermia. 2 case reports].
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Accidents↗
Biomedical subjects
D A Hallbäck
Publications and source records attributed to D A Hallbäck.
Tissue osmolality in intestinal villi of four mammals in vivo and in vitro.
Using a freezing point depression method osmolality in the intestinal tissue of four mammals (gerbils, guinea-pigs, rabbits and rats) was estimated in vivo, during fluid transport from an isotonic electrolyte-glucose solution. Net fluid transport was also measured. In gerbils, guinea-pigs and rabbits tissue osmolality was also estimated during in vitro conditions. A marked hyperosmolality was observed in vivo in the upper parts of the villi of all four mammals studied. The tissue osmolality was significantly higher than that seen in the same species during in vitro conditions. A villus hyperosmolality was observed also in species which exhibited a net fluid secretion (guinea-pig, rabbit ileum), indicating that the fluid secretion emanated from the intestinal crypts. Based on the results of the present experiments and on observations made in earlier experiments performed on the cat, it is proposed that the villus hyperosmolality is created by a countercurrent multiplier present in the intestinal villus. The hyperosmolar compartment in the villus tissue creates the force that drives fluid from lumen to tissue.
Animals↗
Nerve-mediated effect of ethanol on sodium and fluid transport in the jejunum of the rat.
The hypothesis tested in this study is whether a potential harmful substance such as ethanol causes secretion in the small intestine and, if so, whether the secretion is mediated via intestinal nerve reflexes or a direct effect on the epithelium. The jejunum of anaesthetized Sprague-Dawley rats was perfused in vivo with a modified Krebs-Henseleit solution. Three per cent ethanol had no significant effect, whereas 8% ethanol in the perfusate elicited a net secretion of fluid and sodium in the intestine. This secretion was reversed by ganglionic blockade with hexamethonium (10 mg/kg intravenously). The ethanol absorption from the perfusate, on the other hand, was not affected by the ganglionic blockade. We concluded that ethanol dose-dependently caused a nerve-mediated secretion of sodium and fluid in the rat small intestine. Ethanol was probably absorbed by diffusion.
Animals↗
Blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine during regional hypotension.
The hemodynamic reactions of the parallel coupled vascular circuits in the cat small intestine were studied before, during and after a two-hour period of intestinal hypotension induced by lowering the intestinal arterial inflow pressure by partially occluding the superior mesenteric artery during a continuous stimulation of the postganglionic nerves to the small intestine. Furthermore, fluid and electrolyte transport and villous tissue osmolality were measured. A histological examination of biopsies taken during and after the hypotensive period was also carried out. The animals were divided into two groups (undamaged and damaged) according to the histological appearance of the intestinal mucosa. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site ("villous"), nonabsorptive site ("crypt") and muscle layer blood flow. Total intestinal blood flow was lower in the damaged group than in the undamaged group during the arterial hypotension. However, absorptive site blood flow was similar in the two groups. Consequently, a significantly larger fraction of blood flow was distributed to the "villi" in the damaged group. Moreover, absorptive site red blood cell flow was only slightly reduced despite the development of mucosal ulcerations. These findings are discussed in relation to the pathophysiology of the mucosal lesions. Net fluid, net sodium and net chloride absorption was unchanged in the undamaged group whereas in the damaged group a marked decrease was observed after lowering the perfusion pressure. The decrease in net sodium absorption was due to a decrease in the lumen to tissue transport of sodium. Thus, the capacity of the small intestine to absorb fluid and electrolytes is unchanged even during a marked arterial hypotension with a pronounced decrease of intestinal blood flow as long as no mucosal damage has developed.
Animals↗
Effects of hemorrhage on intramural blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the cat small intestine.
The hemodynamic response in the parallel-coupled vascular sections of the cat small intestine were studied before, during and after a two hour period of hemorrhage (about 30 per cent of estimated blood volume). Fluid and electrolyte transport and villous tissue osmolality were also measured. Biopsies for histology were taken at the end of all experiments. The animals were divided in two groups, undamaged and damaged, according to the degree of mucosal damage observed. The hemodynamic reactions were investigated with a method that made it possible to study total intestinal, absorptive site ("villous"), nonabsorptive site ("crypt") and muscle layer blood flows. Total intestinal blood flow was lower in the damaged as compared to the undamaged group during hypovolemia. No difference in absorptive site blood flow was observed between the two groups during hypovolemia. Furthermore, no decrease of red blood cell flow in the "villi" was recorded in either group after hemorrhage. Consequently, mucosal lesions developed despite an unchanged oxygen transport capacity to the villi. The pathophysiology of the mucosal lesions is briefly discussed. Net fluid and sodium absorption was after hemorrhage increased in the undamaged group reflecting a decrease in the tissue to lumen transport of sodium. After retransfusion net fluid and sodium absorption returned to control. In the damaged group, however, net fluid and sodium absorption was decreased after hemorrhage. The increased rate of fluid and electrolyte transport observed in the undamaged small intestine after hemorrhage, is proposed to be an important mechanism for fluid replacement after hemorrhage.
Acid-Base Equilibrium↗
The effect of splanchnic nerve stimulation on blood flow distribution, villous tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.
The effect of splanchnic nerve activation on intestinal fluid transport and intramural blood flow distribution was examined in the cat. Previous reports from our laboratory have demonstrated that splanchnic nerve activation increases fluid absorption. The present study was performed to elucidate the mechanisms behind this effect. The results showed an increase in net sodium and chloride transport on splanchnic nerve activation whether intestinal blood flow decreased or not. The effect on sodium transport was due to a decrease in lumen to tissue flux. The effect could not be explained by a decrease in local blood flow, as it was present despite constant blood flow in both the villous and crypt regions. No change was seen in the villous osmolality gradient on splanchnic nerve activation. On the basis of these findings, it is proposed that the in vivo effect of splanchnic nerve activation is due to a decrease in fluid and electrolyte secretion, probably occurring in the intestinal crypts.
Animals↗
Evidence for cholera secretion emanating from the crypts. A study of villus tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.
Villus tissue osmolality and fluid and electrolyte transport were measured in intestinal segments exposed to cholera toxin. The osmolality of the luminal fluid was kept at about 100, 300, or 600 mOsm X kg-1 by use of appropriate concentrations of mannitol. A net fluid secretion was seen in all experiments, the magnitude being dependent on the osmolality in the lumen. A secretion of sodium, potassium, and chloride was also seen in all experiments but the secretion rate of electrolytes was independent of the osmolality in the intestinal lumen. The hydraulic conductivity of the villus epithelium, calculated from the lumen and tissue osmolality, was the same as that estimated in the normal intestines. A villus tissue osmolality gradient was apparent in all experiments regardless of the mannitol concentration in the lumen, the tip osmolality being hypertonic while the tissue osmolality at the base was isotonic. This was the case also when the luminal fluid was hypotonic, a finding opposite to what we found in an earlier study on the normal feline intestine. A likely explanation for this observation is that the crypts of Lieberkühn secrete fluid containing sodium chloride, which is absorbed by the villus epithelial cells. Hence, a luminal "circulation" of electrolytes between crypts and villi was suggested in the present experimental circumstances.
Animals↗
Villous tissue osmolality, water and electrolyte transport in the cat small intestine at varying luminal osmolalities.
Villous tissue osmolality and net transport for water, sodium, potassium and chloride were determined in the feline small intestine when exposing the mucosa to solutions with different mannitol concentrations (0, 100, 315 and 600 mmol/l). Tissue osmolality at the villous tip varied with luminal osmolality. At the villous base, on the other hand, tissue osmolality remained around the plasma osmolality regardless of the osmolality of the luminal fluid. Transport rates for water were affected in the way predicted from the lumen to tissue osmolality difference. A net flux from tissue to lumen was always recorded for the studied electrolytes. The hydraulic conductivity (Lp) of the intestinal epithelium with dilated intercellular spaces was estimated from the present results to be around 30 x 10(-12) cm x s-1 x Pa-1. When the intercellular spaces were collapsed Lp was estimated to be 15 x 10(-12 cm x s-1 x Pa-1.
Animals↗
Vascular anatomy and tissue osmolality in the filiform and fungiform papillae of the cat's tongue.
The vascular anatomy of the filiform and fungiform papillae of the feline tongue was studied by i.a. injection of India ink. Vascular loops of various appearances were found in the types of papillae studied, i.e. the large and the small filiform papillae and the fungiform ones. Such hairpin loops may function as countercurrent exchangers and to test this hypothesis tissue osmolality was determined in the papillae, while exposing them to various isotonic electrolyte solutions. The large filiform papillae with a vascular arrangement similar to that of intestinal villi exhibited a marked osmolar gradient from tip to base when exposed to a solution containing both glucose and sodium. If sodium and/or glucose was excluded from the solution, tissue osmolality was significantly decreased. This was also the case when the chloride ions of the solution was substituted with sulphate. The small filiform papillae are only provided with one or a few capillary loops. They exhibited a less marked osmolar gradient than the large ones and one of the different electrolyte solutions decreased the gradient. In the fungiform papillae a tissue hyperosmolality at the tip was also demonstrated. It is proposed that the papillary epithelium is provided with active transport mechanism(s) and that the papillary vessels function as countercurrent multipliers. The functional importance of these mechanisms are tentatively discussed.
Animals↗
Importance of sodium and glucose for the establishment of a villous tissue hyperosmolality by the intestinal countercurrent multiplier.
The intestinal countercurrent multiplier has earlier been shown to create an increased tissue osmolality in the villi (Jodal et al. 1978). In the present paper the importance of varying the luminal contents on the creation of the villous hyperosmolality was investigated using the cryoscopic technique described by Jodal et al. (1978). The perfusion solutions used contained 0, 25 or 147 mmol Na/l and were either provided with mannitol or glucose (30 mmol/l). It was demonstrated that sodium was of particular importance for the establishment of the villous hyperosmolality while glucose only contributed significantly at low luminal sodium concentrations. It is therefore proposed that glucose only in the absence of sodium in the luminal perfusate may effectively participate in the generation of the villous tissue hyperosmolality via the countercurrent multiplication mechanism.
Animals↗
Villous tissue osmolality and intestinal transport of water and electrolytes.
The villous tissue hyperosmolality created by the intestinal countercurrent multiplier has been proposed to be of importance for fluid transport across the intestinal epithelium in vivo. This study was performed to test this hypothesis. Net transport of fluid and electrolytes (sodium, potassium and chloride), as well as unidirectional fluxes of water and sodium were determined in the small intestine of the cat. The villous osmolality was altered by varying the composition of sodium and glucose in the isotonic solutions perfusing the intestinal lumen. Net transport of fluid was correlated to tissue osmolality mainly due to an increase of the unidirectional flux of water from lumen to tissue with augmented tissue osmolality. The results are thus consistent with the view that the intestinal countercurrent multiplier is of essential importance for net water transport. A correlation was found between net water and net sodium intestinal transport. A similar correlation was also demonstrated between net sodium and net chloride absorption rates in the jejunum while in the ileum net loss of sodium into the intestinal lumen was not accompanied by any corresponding loss of chloride ions. This observation suggests the presence of a sodium independent transport mechanism for chloride in the ilium but not in the jejunum.
Animals↗
Effects of cholera toxin on villous tissue osmolality and fluid and electrolyte transport in the small intestine of the cat.
The effects of cholera toxin on tissue osmolality and on net transport rates of water, sodium, chloride and potassium as well as on unidirectional fluxes of water and sodium were studied in vivo. In all experiments the toxin caused a net secretion of water, sodium, chloride and potassium. The unidirectional sodium transport from tissue to lumen was increased while the flux in the opposite direction was reduced 180 min after cholera toxin instillation. Cholera toxin produced only a small reduction in the villous tissue hyperosmolality, created by the intestinal countercurrent exchanger. This reduction was far too small to explain the observed net secretion of fluid and solutes induced by the cholera toxin. Other mechanisms underlying the cholera secretion are discussed.
Animals↗
Tissue osmolality in intestinal villi during luminal perfusion with isotonic electrolyte solutions.
A cryoscoptic technique has been developed that makes it possible to determine tissue osmolality in the core of the intestinal villi. During absorption from an isotonic electrolyte solution containing glucose an osmolality gradient was demonstrated from tip to base of the villi in both the jejunum and the ileum. The tissue osmolality at the villous tips was measured to 1 000-1 200 mOsm/kg H2O while the osmolality at the villous base was approximately isotonic with plasma. Increasing intestinal blood flow by i.a. administration of a vasodilator drug, or making the intestine ischemic by clamping the intestinal vascular supply while supplying the mucosa with oxygen, markedly decreased tissue osmolality. Substituting all sodium ions with choline in the luminal perfusate abolished almost completely the tissue hyperosmolality and the intestine became a secretory organ. These observations are consistent with the view that the observed villous tissue hyperosmolality was created by a countercurrent multiplication of sodium chloride. The physiological implications of this mechanism is discussed and it is, among other things, proposed that the hyperosmolar region represents the hyperosmotic compartment necessary for explaining intestinal water absorption.
Animals↗
The effects of cholera toxin on intramural blood flow distribution and capillary hydraulic conductivity in the cat small intestine.
Blood flow distribution to the mucosa-submucosa and to the muscularis in the cat small intestine was investigated with a 85Kr elimination technique before and after exposing the intestinal mucosa for 30 min to cholera enterotoxin. In all experiments the toxin induced an intestinal secretion. Concomitantly, total intestinal blood flow was increased to a level 50 per cent above control 3 h after exposure. This vasodilatation reflected a doubling of mean blood flow in the mucosa--submucosa while muscularis blood flow remained unchanged. In another series of experiments the effect of cholera toxin on intestinal capillary hydraulic conductivity was investigated by determining the capillary filtration coefficient (CFC). A slight increase in CFC was noted during the 3 h observation period but this was not more pronounced than would have been expected from the concomitant vasodilatation. It is concluded that hemodynamic changes in the intestinal mucosa may be one of the several factors that probably are involved in the pathogenesis of cholera.
Animals↗
Evidence for the existence of a countercurrent exchanger in the small intestine in man.
The vasculature in the human villus forms vascular loops by the supplying arterial vessel and the draining capillaries and/or veins. This study reports two experimental observations that strongly suggest that these vascular loops function as countercurrent exchangers. (1) The elimination of intraarterially injected 85Kr from the human small bowel exhibits an initial very rapid component of the type earlier reported in the feline gut. This component in all probability reflects the extravascular "shunting" in the exchanger of the injected radioactive tracer. (2) When exposing the intestinal mucosa to an isotonic electrolyte solution containing glucose, an osmolality gradient from the tip to the base of the human villi was demonstrated, the tips having an osmolality of around 700 milliosmoles per kg H2O. This hyperosmolality is created by the exchanger acting as a countercurrent multiplier.
Colon↗
A method for the continuous study of net water transport in the feline small bowel.
A new perfusion technique has been developed for the study of net water transport across the intestinal epithelium in vivo. The lumen of an isolated intestinal segment is steadily perfused with a solution of known composition in a closed perfusion system with a reservoir large enough to prevent recirculation. The intestinal segment may be enclosed in a plethysmorgraph. Changes in the perfused volume is recorded by a volume transducer coupled to the recirculating system via a T-tube. If no motility occurs, the changes of the perfusion volume reflects net water transport across the intestinal epithelium. A quantitative comparison of this technique with the convention polyethylene glycol method revealed no significant difference. The plethysmorgraphic method also makes it possible to quantify the net water absorption via lymph and blood.
Animals↗